Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP89 | DOI: 10.1530/endoabs.37.EP89

ECE2015 Eposter Presentations Adrenal cortex (94 abstracts)

Low DHEAS: a sensitive and specific screening test for the detection of subclinical hypercortisolism in adrenal incidentalomas

Michael Conall Dennedy 1, , Anand K Anamalai 1 , Olivia Prankerd Smith 1 , Andrew S Powlson 1 , Johann Graggaber 1 , Ashley Shaw 2 , David J Halsall 3 & Mark Gurnell 1


1Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke’s Hospital, University of Cambridge and National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge, UK; 2Departments of Radiology, Addenbrooke’s Hospital, University of Cambridge and National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge, UK; 3Departments of Clinical Biochemistry, Addenbrooke’s Hospital, University of Cambridge and National Institute for Health Research Cambridge Biomedical Research Centre, Cambridge, UK; 4Discipline of Pharmacology & Therapeutics (MCD), National University of Ireland, Galway, Galway, Ireland.


Subclinical hypercortisolism (SH) occurs in 5–30% of incidentally-detected adrenal adenomas (AIs). Common screening tests for ACTH-independent hypercortisolism have significant false positive rates, mandating further investigations that are both time and resource intensive. We investigated whether a low basal DHEAS level is a sensitive and specific screening test for the detection/exclusion of SH in patients with newly-diagnosed AI. We recruited 185 consecutive patients with AI referred to our clinic between 2006 and 2013 were screened for clinical and biochemical evidence of adrenal medullary and cortical (1 mg dexamethasone suppression test, 24 h urinary free cortisol (UFC), serum DHEAS, plasma renin and aldosterone) hyperfunction. All positive dexamethasone suppression (>1.8 μg/dl (50 nmol/l)) and UFC (> upper limit of reference range) results were further investigated, and we diagnosed SH when at least two of the following criteria were met: raised UFC, raised midnight serum cortisol, 48 h dexamethasone suppression test cortisol >1.8 μg/dl (50 nmol/l). Plasma ACTH was <10 pg/ml (2.2 pmol/l) in all patients with SH. At presentation, 29 patients (16%) were diagnosed with SH. We calculated an age-and gender-specific DHEAS ratio (derived by dividing measured DHEAS by the lower limit of the respective reference range) for all patients in the cohort and found that a ratio ≤1.12 was a sensitive (100%) and specific (91.9%) screening test for the diagnosis of SH. In comparison, a cortisol level after a 1 mg dexamethasone suppression test of 1.9 μg/dl (53 nmol/l) was a sensitive (100%) screening test for SH, but had lower specificity (82.9%). 24 h UFC lacked sensitivity (69%) and specificity (68%). A single basal measurement of DHEAS offers comparable sensitivity and greater specificity to the existing gold-standard 1 mg dexamethasone suppression test for the detection of SH in patients with AIs.

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